In this year, we were focused on three major sub-projects. First, using high-speed monitoring of EEG and EMG in freely moving rats, we demonstrated that intravenous (iv) cocaine induced rapid cortical EEG desynchronization and motor activation that occur within the time-course of injection. We also showed that a similar rapid response could be elicited by both cocaine-methiodide that cannot cross the blood-brain barrier and procaine that has virtually no activity with respect to monoamine transporters. Therefore, it appears that rapid activation induced by iv cocaine is triggered via activation of peripheral non-monoamine neural substrates. Currently, we are expanding this neurophysiological/neuropharmacological approach to study rapid effects of nicotine, another major drug of abuse. While the action on centrally located nicotinic receptors is critical for drugs reinforcing properties, this drug could also activate numerous peripherally located nicotinic receptors, thus providing a rapid sensory signal from the periphery and affecting central neurons. The final third sub-project, which was initiated during this year, is focused on reliable detection of glutamate (GLU) in the brain of freely moving rats. Currently, we are working to resolve several technical problems related to the use and performance of enzyme-coated electrochemical electrodes. Since GLU transmission is essential for normal behavioral activity and stable alterations of GLU transmission could occur following drug addiction, our first goal is to examine GLU release following exposure to various environmental stimuli and addictive drugs. This work will be expanded during the next years to include other detected substances and the use of more complicated behavioral paradigms that involve the use of addictive drugs.